Atheroembolic Kidney Disease
In atheroembolic kidney disease, numerous small pieces of fatty material (atheroemboli) travel from arteries above the kidneys to clog the smallest branches of the renal arteries, causing the kidneys to fail. Tiny pieces of hard fatty material adhering to a hardened (atherosclerotic) blood vessel wall, usually the aorta, break off and travel through the bloodstream, becoming emboli (atheroemboli). Some emboli travel to the smallest renal arteries, blocking parts of the kidney's blood supply. Usually, this process affects both kidneys about equally and at the same time. The fatty material may break off spontaneously when there is severe atherosclerosis of the aorta. It more commonly occurs as a complication of surgery or angioplasty or of imaging procedures that involve the aorta, such as arteriography, when pieces of fatty material adhering to the walls of the aorta are unintentionally broken off. Atheroembolic kidney disease is much more common in older people. Symptoms Atheroembolic kidney disease usually produces acute or slowly progressive failure of the kidneys. If the blockage of arteries results from a surgical or imaging procedure involving the aorta, the kidneys often fail suddenly. Urine production is often decreased. As the duration and severity of kidney failure increase, various symptoms may appear, beginning with fatigue, nausea, loss of appetite, itching, and difficulty concentrating. The symptoms reflect disturbances in the muscles, brain and nerves, heart, digestive tract, and skin that result from kidney failure. Atheroemboli may cause symptoms in other organs. If atheroemboli travel to the arms or legs, such symptoms as blue toes or a lacy purplish discoloration of the skin and even gangrene may result. Pieces of atheroemboli that travel to an eye may cause sudden blindness. Diagnosis An imaging test may be done to exclude the possibility of renal artery blockage, which can sometimes cause similar symptoms. A kidney biopsy is the best way for doctors to make the diagnosis of atheroembolic kidney disease. A tissue sample examined with a microscope shows characteristic evidence of fatty material in the smallest arteries. Examination of skin or muscle specimens may also help to establish the diagnosis. Prognosis and Treatment In the past, people with atheroembolic kidney disease tended to die within weeks or months. However, more recently, treatment has improved. Most people live at least a year. About half live 4 years or more. The treatment is to support the person as well as possible. For example, high blood pressure is treated. Dialysis may be needed during kidney failure, but sometimes the kidneys eventually resume functioning.
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Blockage of the Renal Arteries
There are two renal arteries—one supplies blood to the right kidney, the other to the left kidney. These arteries branch into many smaller arteries. A gradual narrowing of one or both of the renal arteries may cause high blood pressure or a worsening of previously controlled high blood pressure. Blood pressure may remain high despite treatment with many antihypertensive drugs. In people who are given an angiotensin-converting enzyme (ACE) inhibitor, an angiotensin II receptor blocker, or a renin inhibitor to treat high blood pressure, kidney function may decline rapidly. The effect is reversible if the drug is stopped promptly. Causes Blockage of the renal artery or one of its large or medium-sized branches is unusual. Most often such blockages occur when a clot moves through the bloodstream from elsewhere in the body (becoming an embolus) and lodges in the renal artery. Typically, such clots originate as fragments from a larger clot in the heart or from the breakup of a fatty deposit (atheroma) in the aorta. Alternatively, a blockage may result when a blood clot forms in the renal artery itself, usually where the artery has been injured. A sudden injury may be caused by a medical procedure, such as surgery, angiography, or angioplasty. A clot may also develop where the renal artery has been gradually injured or damaged by atherosclerosis, arteritis (inflammation of arteries), or an aneurysm (a slow-forming bulge in the wall of the artery). A tear in the lining of the aorta or the renal artery can cause a sudden obstruction of blood flow; a tear may also cause the artery to rupture. Diseases that cause the walls of arteries to become thicker and less elastic because of deposits of fatty material (atherosclerosis) or the development of fibrous material (fibromuscular dysplasia) may predispose vessels to tears. These disorders can lead to significant narrowing and partial blockage of the renal arteries even when there is no blood clot. When narrowing or blockage occurs but no blood clot exists, the condition is called renal artery stenosis. Symptoms A partial blockage of the renal arteries usually does not cause any symptoms. If blockage is sudden and complete, the person may have a steady aching pain in the lower back or occasionally in the lower abdomen. A complete blockage may cause fever, nausea, vomiting, and back pain. Rarely, a blockage causes bleeding that turns the urine red or dark brown. Complete blockage of both renal arteries—or of one renal artery in people who have only one kidney—completely stops urine production and shuts down the kidneys (a condition called acute kidney failure). If a blockage is the result of a clot that has moved to and lodged in one of the renal artery branches, the person may have clots elsewhere in the body, such as in the intestine, brain, and the skin of the fingers and toes. These clots may cause pain in these areas as well as small ulcers or gangrene, or a small stroke. Diagnosis Doctors may suspect a blockage because of the symptoms. Laboratory tests, such as a complete blood count and urinalysis (microscopic examination of the urine), may add further clues. Because none of the symptoms or laboratory tests can specifically identify a blockage, doctors need to perform imaging tests of the kidneys to demonstrate that they are not functioning properly. Computed tomography (CT) angiography, magnetic resonance (MR) angiography, Doppler ultrasonography, and an isotope perfusion scan can show absent or diminished blood flow to the affected kidney. All of these tests have advantages and disadvantages. For example, CT angiography and MR angiography are very accurate. However, CT angiography involves using an intravenous radiopaque dye (contrast agent) that increases the risk of kidney damage in people with decreased kidney function. MR angiography involves use of an intravenous contrast agent (gadolinium) that increases the risk of nephrogenic systemic fibrosis in people with decreased kidney function. Nephrogenic systemic fibrosis causes scar tissue to form throughout the body and is not easily reversed or cured. Arteriography is the most accurate test doctors can use to confirm the diagnosis. With arteriography, a catheter is inserted into an artery, which occasionally causes injury to the artery. In addition, as with CT angiography, arteriography involves use of a radiopaque dye that increases risk of kidney damage. Arteriography is done only if doctors are considering surgery or angioplasty to relieve the blockage. Doctors may monitor how well kidney function recovers by repeating ultrasound , radionuclide scanning, or blood tests that measure kidney function at frequent intervals. Prognosis Although kidney function may improve with treatment, it usually is not restored completely. The outlook is poor when the artery is blocked by clots that have formed in other parts of the body (such as the heart). Clots from that source are likely to travel to other parts of the body (such as the brain or intestine) and cause problems there. Treatment Treatment is aimed at preventing further deterioration of blood flow and restoring blood flow that has been blocked. In the case of blood clots, the usual treatment is with anticoagulant drugs (see Bleeding and Clotting Disorders: Drugs and Blood Clots: A Complicated Relationship ). These drugs are given first intravenously and then by mouth for longer periods of time. Anticoagulants prevent the initial clot from enlarging and additional clots from forming. Drugs that dissolve clots (fibrinolytics or thrombolytics—see Bleeding and Clotting Disorders: Drugs and Blood Clots: A Complicated Relationship) may be more effective than anticoagulants. However, fibrinolytic drugs improve kidney function only when the artery is not completely blocked or when clots can be dissolved quickly. After 30 to 60 minutes of complete blockage, permanent damage is likely. However, fibrinolytic drugs can be helpful only if given within 3 hours. Surgery is sometimes done to open an artery blocked by a clot, but this treatment has a greater risk of complications and death and does not improve kidney function more than anticoagulant or fibrinolytic drugs alone. Drug treatment is almost always preferred to surgery. However, when the cause is injury, the artery must be surgically repaired. To relieve a blockage caused by atherosclerosis or fibromuscular dysplasia of a renal artery, doctors may thread a balloon catheter from the femoral artery in the groin to the renal artery. The balloon is then inflated to force open the obstructed area. This procedure is called percutaneous transluminal angioplasty. When doctors perform this procedure, they may place a short hollow tube (stent) in the artery to prevent the blockage from occurring again. When angioplasty is unsuccessful, surgery may be considered to remove or bypass a blockage caused by atherosclerosis or fibromuscular dysplasia.
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Malignant Hypertensive Nephrosclerosis
In malignant hypertensive nephrosclerosis, severe high blood pressure (malignant hypertension) damages the smallest arteries in the kidneys, and kidney failure progresses rapidly. Malignant hypertensive nephrosclerosis occurs in about 1 out of 200 people with high blood pressure and is more common among blacks than whites. It is most common in men during their 40s and 50s and women during their 30s. High blood pressure (hypertension) causes damage to body organs. However, usually the damage takes months or years to develop. In malignant hypertension, organ damage develops over hours or days. Because hypertension causes damage so rapidly, it is described as malignant, but in this case, malignant does not mean cancerous. Malignant hypertension most commonly results from poorly controlled high blood pressure. It may also result from other conditions, such as glomerulonephritis, chronic kidney failure, narrowing of the renal artery causing renovascular hypertension, inflammation of renal blood vessels (vasculitis), or, rarely, hormonal disorders such as pheochromocytoma, primary aldosteronism, or Cushing's syndrome. Symptoms Symptoms initially are caused by the effects of the severe high blood pressure on the brain, eye, and heart. Some symptoms, which may include restlessness, blurred vision, headache, nausea, vomiting, sleepiness, and confusion, result from swelling of brain and eye tissue. Seizures and coma may also occur if swelling is severe or if there is bleeding within the brain. Heart failure may cause difficulty breathing. Damage to the kidneys eventually produces the symptoms of kidney failure, such as fatigue, weakness, and itching. Diagnosis Malignant hypertensive nephrosclerosis is likely in people who have malignant hypertension and symptoms of kidney failure or laboratory evidence of kidney failure. By viewing the back of the eye with an ophthalmoscope, doctors can see areas of bleeding, collections of fluid, and swelling of the optic nerve. Doctors may also detect heart enlargement and heart strain or failure. These findings in the eye and heart indicate malignant hypertension. Blood tests show elevated levels of creatinine and urea nitrogen, indicating kidney failure. Protein leaking from the kidneys can be detected in the urine, along with blood cells. Anemia often results from the breakdown and impaired production of red blood cells. Widespread clotting within the blood vessels is also common (disseminated intravascular coagulation—see Bleeding and Clotting Disorders: Disseminated Intravascular Coagulation (DIC)). Blood levels of substances produced by the kidneys that help regulate blood pressure (renin and aldosterone) are extremely high. Prognosis If malignant nephrosclerosis is not treated, 40 to 80% of people die within one year. However, with the best medical care, including rigorous control of high blood pressure with diet and drugs and treatment of the kidney failure, average survival can be up to 12 years. People who have less severe kidney failure improve the most with treatment. Treatment Treatment includes aggressive lowering of blood pressure with drugs. Lifestyle changes (for example, diet and exercise) also help lower blood pressure but rarely enough without drugs. Treating the kidney failure is also essential. Occasionally, people improve enough that dialysis can be stopped.
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Renal Cortical Necrosis
enal (kidney) cortical necrosis is death of the tissue in the outer part of kidney (cortex) that results from blockage of the small arteries that supply blood to the cortex and that causes acute kidney failure. Renal cortical necrosis can occur at any age. About 10% of the cases occur in infants and children. More than half of the newborns with this condition had deliveries complicated by premature detachment of the placenta. The next most common cause is a bacterial infection of the bloodstream (sepsis). In children, renal cortical necrosis may follow severe infection, severe dehydration, shock, or the hemolytic-uremic syndrome (see Bleeding and Clotting Disorders: Thrombocytopenia (ITP, TTP)). In adults, sepsis causes one third of all cases of renal cortical necrosis. Other causes in adults include rejection of a transplanted kidney, burns, inflammation of the pancreas, injury, snakebite, use of certain drugs, and poisoning from certain chemicals. About half of the cases in women follow complications of pregnancy, such as premature detachment of or abnormal position of the placenta, bleeding from the uterus, infections immediately after childbirth, blockage of arteries by amniotic fluid, death of the fetus within the uterus, and preeclampsia. Symptoms The urine often becomes red or dark brown because of the presence of blood. Pain along both sides of the lower back may occur. A fever is often present. Changes in blood pressure, including mildly high pressure or even low pressure, are common. Urine flow may slow or stop. Diagnosis Doctors may have difficulty making a diagnosis of renal cortical necrosis because it may resemble other types of acute kidney failure. Doctors may suspect renal cortical necrosis based on symptoms in people who have predisposing conditions. The diagnosis is often confirmed with an imaging test such as computed tomography (CT) angiography. Kidney biopsy can give doctors the most accurate diagnostic information, but a biopsy involves removing kidney tissue and may be unnecessary if the diagnosis is evident. Thus, biopsy is not done in most people. Blood tests may reveal abnormally shaped red blood cells circulating in the blood. The small amount of urine that is produced contains protein and many white and red blood cells, along with kidney cells and other debris. Prognosis and Treatment In recent years, with improved treatment, prognosis has improved. About 80% of people live a year or longer, although most people need permanent dialysis or kidney transplantation. Treatment is supportive care, which may involve giving intravenous fluids, blood transfusion, antibiotics, dialysis, or a combination.
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Renal Vein Thrombosis
Renal vein thrombosis is blockage of the renal vein, which carries blood away from the kidney, by a blood clot. In adults, renal vein thrombosis usually occurs with other kidney disorders that cause the nephrotic syndrome, in which large amounts of protein are lost in the urine. Renal vein thrombosis may also be caused by kidney cancer or conditions that put pressure on the renal vein (for example, a tumor) or on the inferior vena cava, which the renal vein drains into. Other possible causes are blood clotting disorders (hypercoagulability disorders), vasculitis, sickle cell disease or diabetes that affects the kidney, oral contraceptive use, injury, cocaine abuse, or, rarely, thrombophlebitis migrans—a condition in which clotting occurs sequentially in different veins all over the body. Symptoms Renal vein thrombosis occurs most often in adults. In adults, onset and progression are usually gradual and without symptoms. An occasional clue to doctors is when a piece of clot breaks off and travels from the renal vein to the lungs (pulmonary embolism—see Pulmonary Embolism (PE): Pulmonary Embolism). This event causes sudden pain in the chest that is made worse by breathing, along with shortness of breath. In other people, urine production diminishes. In most children and a limited number of adults, onset and progression are usually sudden. Pain, often the first symptom, typically occurs in the back behind the lower ribs and in the hips. The person may have fever, less than a normal amount of urine, and blood in the urine. Diagnosis Blood tests may indicate evidence of kidney failure. Computed tomography (CT) angiography and magnetic resonance (MR) angiography are the tests doctors use to diagnose renal vein thrombosis. They are highly accurate and do not require insertion of a catheter into an artery or a vein deep in the body, so they are usually the preferred tests. Ultrasonography is not as accurate, but it is very safe. An ultrasound scan shows enlarged kidneys if the blockage developed suddenly. Doppler ultrasonography may show that there is no blood flowing in the kidney vein. X-rays of the inferior vena cava or the renal vein that are taken after a radiopaque dye is injected into an artery or deep vein (venography) is the most accurate test, but may cause clots to break off and travel through the bloodstream, becoming emboli, which can cause complications. Prognosis The outcome depends on the cause of the thrombosis, complications, and the degree of kidney damage. Death from renal vein thrombosis is rare and usually results from a fatal underlying disorder or from complications, such as a pulmonary embolism. The effects on kidney function depend on whether one or both kidneys are affected, whether blood flow is restored, and what the state of kidney function was before the blockage occurred. Treatment The primary treatment is with anticoagulant drugs, which usually improve kidney function by preventing the formation of additional clots and reducing the risk of pulmonary embolism. Use of drugs that dissolve clots (fibrinolytics) is a newer treatment that is becoming more widespread but is still not routine. Rarely, surgery is done to remove clots in the renal vein. A kidney is rarely removed and then only if other complications, such as high blood pressure, develop. |
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